Computed tomography (CT) has revealed that many demented patients with a clinical diagnosis of Alzheimer's disease display more marked cerebral atrophy than expected for their age (DeCarli et al "Critical analysis of the use of computer-assisted transverse axial tomography to study human brain in aging and dementia of the Alzheimer type," Neurology 1990; 40:872-883). Functional changes in demented patients have been found by methods such as positron emission tomography (PET) and single photon emission tomography (SPET) that show cerebral blood flow, glucose or oxygen uptake, or uptake of radioligands: the most frequent finding is a functional deficit in the posterior parietal and temporal lobes of the cortex (Hoffman et al "&lt;F-18&gt;-Fluorodeoxyglucose (FDG) and positron emission tomography (PET) in aging and dementia--A decade of studies," Eur. Neurol., 1989;29:16-24; McGeer et al, "Fluorodeoxyglucose-18 positron emission tomography studies in presumed Alzheimer cases, including 13 serial scans," Canad. J. Neurol. Sci., 1990; 17:1-11; Prohovnik et al, "Cerebral perfusion as a diagnostic marker of early Alzheimer's disease," Neurology 1988;28:931-937; Perani et al, "Technetium-99m-HMPAO-SPECT study of regional cerebral perfusion in early Alzheimer's disease," J. Nucl. Med. 1988;29:1507-1514) Single photon emission tomography (SPET) has recently been used to show that the functional deficits in the posterior parietal and lateral temporal lobes (as indicated by reduced blood flow) are related to the degree of cognitive decline (Burns et al, "The investigation of Alzheimer's disease with single photon emission tomography," J. Neurol. Neurosurg. Psychiat., 1989;52:248-253; Hunter et al, "The pattern of function-related regional cerebral blood flow investigated by single photon emission tomography with Tc-99M-HMPAO in patients with presenile Alzheimer's disease and Korsakoff's psychosis," Psychol. Med., 1989;19:847-855; Montaldi et al, "Measurements of regional cerebral blood flow and cognitive performance in Alzheimer's disease," J. Neurol. Neurosurg. Psychiat., 1990;53:33-38). Such findings are difficult to reconcile with neuropathological studies which show that the most severely affected parts of the brain in Alzheimer's disease are in the medial temporal lobe, mainly the amygdala, the hippocampal formation and adjacent parahippocampal gyrus as indicated by a high concentration of plaques and tangles and reduced tissue mass (Brun et al, "Regional pattern of degeneration in Alzheimer's disease: neuronal loss and histopathological grading," Histopathology, 1981;5:549-564; Wilcock et al, "Plaques, tangles and dementia. A quantitative study," J. Neurol. Sci., 1982;56:343-356; Hyman et al, "Cell-specific pathology isolates the hippocampal formation," Science, 1984;225:1168-1170; Ball et al, "A new definition of Alzheimer's disease: a hippocampal dementia," Lancet, 1985;i:14-16; Esiri et al, "A quantitative study of the neurofibrillary tangles and the choline acetyltransferase activity in the cerebral cortex and the amygdala in Alzheimer's disease," J. Neurol. Neurosurg, Psychiat., 1990;53:161-165). Atrophy of these areas can be revealed in life by CT studies in which the scan angle is adjusted to give a clearer view of the medial temporal lobe. Such studies on patients with a clinical diagnosis of Alzheimer's disease have indeed shown severe damage to structures in the medial temporal lobe (LeMay, M., "CT changes in dementing diseases: a review," Amer. J., Neuroradiol. 1986;7:841-853; Kido et al, "Temporal lobe atrophy in patients with Alzheimer disease: a CT study," Amer. J. Neuroradiol., 1989;10:551-555; de Leon et al, "Early marker for Alzheimer's disease: the atrophic hippocampus," Lancet 1989;ii:672-673; George et al, "CT diagnostic features of Alzheimer's disease: importance of the choroidal/hippocampal fissure comples," Amer. J. Neuroradiol, 1990;11:101-107). However, atrophy of the medial temporal lobe is also found in other conditions, notably epilepsy and hypoxia (Esiri and Oppenheimer, "Diagnostic Neuropathology," Oxford, Blackwell Scientific Publications, 1989), schizophrenia (Roberts, G. W., "Schizophrenia--The cellular biology of a functional psychosis," Trends Neurosci., 1990;13:207-211), amnesia (Press et al, "Hippocampal abnormalities in amnesic patients revealed by high-resolution magnetic resonance imaging," Nature, 1989;341:54-57) and, perhaps, depression (Bowen et al, "Circumscribed changes of the cerebral cortex in neuropsychiatric disorders of later life," Proc. Nat. Acad. Sci. USA, 1989;86: 9504-9508) and so is not unique to dementia of Alzheimer's type.
The CT and SPET studies described above have each been carried out on different groups of patients and not on the same patients.